一氧化氮、血栓素/前列环素及ATP与肝硬变大鼠肝脏缺血再灌注损伤

THE ROLE OF NITRIC OXIDE, TXA 2/PGI 2 AND ATP ON HEPATIC ISCHEMIA/REPERFUSION INJURY IN CIRRHOTIC RATS

四氯化碳复制大鼠肝硬变模型，通过大鼠肝脏缺血再灌注损伤模型，比较硬变肝与正常肝在缺血再灌注损伤时的差异和意义。结果显示：肝硬变时对缺血再灌注损伤反应与正常大鼠不同，再灌注时肝脏一氧化氮合成释放显著增加，肝组织ＡＴＰ含量明显降低且长时间难以恢复等，可能是肝硬变时对缺血再灌注损伤更敏感、更易发生肝功能衰竭的重要原因。

The aim of this study is to assess ischemia/reperfusion injury in carbon tetrachloride induced cirrhotic liver as compared to normal liver in the rats. Results showed that in cirrhotic liver, instead of diminishing the hepatic vein nitric oxide level increased significantly after ischemia from 8.04 μmol/L to 11.52 μmol/L and remained high till 5 hrs after reperfusion. The hepatic adenosine triphosphate (ATP) contents decreased as that seen in normal rat but did not restore to normal till the end of 5 hrs after reperfusion. Based on these findings, it is postulated that in cirrhotic liver, ischemia/reperfusion injury is aggrvated as evidenced by of nitric oxide, and extended diminishing in ATP.